Linked Life Data

10580415

Source:http://linkedlifedata.com/resource/pubmed/id/10580415

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
1999-12-13
pubmed:abstractText
Leptin, an ob gene product, has been shown to suppress food intake by regulating hypothalamic neuromodulators. The present study was designed to examine the involvement of brain histamine in leptin-induced feeding suppression. A bolus infusion of 1.0 microg leptin into the rat third cerebroventricle (i3vt) elevated the turnover rate of hypothalamic neuronal histamine (P < 0.05) as assessed by pargyline-induced accumulation of tele-methylhistamine (t-MH), a major metabolite of histamine. No remarkable change in the mRNA expression of histidine decarboxylase (HDC), a histamine-synthesizing enzyme, was observed in the hypothalamus after i3vt infusion of leptin. These results indicate that leptin increases histamine turnover by affecting the posttranscriptional process of HDC formation or histamine release per se. As expected, concomitant suppression in 24-h cumulative food intake was also observed after infusion of leptin. Systemic depletion of brain histamine levels by pretreatment with an intraperitoneal injection of 224 micromol/kg alpha-fluoromethylhistidine (FMH), a suicide inhibitor of HDC, attenuated the leptin-induced feeding suppression by 50.7% (P < 0.05). This attenuation of feeding suppression was mimicked by the i3vt infusion of 2.24 micromol/kg FMH before leptin treatment (P < 0.05). In addition, concentrations of hypothalamic histamine and t-MH were lowered in diabetic (db/db) mice, which are known to be deficient in leptin receptors (P < 0.05 vs. lean littermates for each amine), although the amine levels were higher in diet-induced obese rats (P < 0.05 for each amine). Leptin-deficient obese mice (ob/ob) showed lower histamine turnover (P < 0.05 vs. lean littermates), which recovered after leptin infusion. Thus, a growing body of results points to an important role for the hypothalamic histamine neurons in the central regulation of feeding behavior controlled by leptin.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0012-1797
pubmed:author
pubmed:issnType
Print
pubmed:volume
48
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2286-91
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:10580415-Animals, pubmed-meshheading:10580415-Cerebral Ventricles, pubmed-meshheading:10580415-Feeding Behavior, pubmed-meshheading:10580415-Gene Expression Regulation, Enzymologic, pubmed-meshheading:10580415-Histamine, pubmed-meshheading:10580415-Histidine Decarboxylase, pubmed-meshheading:10580415-Hypothalamus, pubmed-meshheading:10580415-Infusions, Parenteral, pubmed-meshheading:10580415-Leptin, pubmed-meshheading:10580415-Male, pubmed-meshheading:10580415-Methylhistamines, pubmed-meshheading:10580415-Mice, pubmed-meshheading:10580415-Mice, Inbred C57BL, pubmed-meshheading:10580415-Mice, Obese, pubmed-meshheading:10580415-Neurons, pubmed-meshheading:10580415-Obesity, pubmed-meshheading:10580415-RNA, Messenger, pubmed-meshheading:10580415-Rats, pubmed-meshheading:10580415-Rats, Wistar, pubmed-meshheading:10580415-Time Factors, pubmed-meshheading:10580415-Transcription, Genetic
pubmed:year
1999
pubmed:articleTitle
Hypothalamic neuronal histamine as a target of leptin in feeding behavior.
pubmed:affiliation
Department of Internal Medicine I, School of Medicine, Oita Medical University, Hasama, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't